Complications after Cranioplasty: A Pictorial Narrative with Techniques to Manage and Avoid the Same

Abstract Background  Cranioplasty following decompressive craniotomy is considered to be a “routine procedure” but several large series have documented a significant amount of both delayed and immediate complications and also a mortality rate of up to 3.6%. Materials and Methods  We went through some of the salient complications (excluding seizures) needing resurgery following interval cranioplasty over the past 18 years at our institution in over 300 cases and analyzed the literature that mention these complications and their treatment. Results  In addition to the commonly mentioned complications, we found some that had been rarely described or not mentioned hitherto in the literature which we have presented as a pictorial narrative. Based on our experience, we recommend some measures that may decrease the incidence or prevent the occurrence of the same. Conclusions  Attention to small but basic surgical techniques will go a long way in preventing unwanted postoperative events.


Introduction
Cranioplasty (CP) following decompressive craniotomy (DC) 1 is performed after the intracranial pressure subsides with the aim of improving cosmesis and neurological function. 2,3 Conventionally done 3 to 6 months after DC, it is termed as "early" CP when done within 12 weeks of DC and "late" if done after this period. 3 Though commonly considered to be a "simple operation"

Abstract
Background Cranioplasty following decompressive craniotomy is considered to be a "routine procedure" but several large series have documented a significant amount of both delayed and immediate complications and also a mortality rate of up to 3.6%.

Materials and Methods
We went through some of the salient complications (excluding seizures) needing resurgery following interval cranioplasty over the past 18 years at our institution in over 300 cases and analyzed the literature that mention these complications and their treatment. Results In addition to the commonly mentioned complications, we found some that had been rarely described or not mentioned hitherto in the literature which we have presented as a pictorial narrative. Based on our experience, we recommend some measures that may decrease the incidence or prevent the occurrence of the same.
Conclusions Attention to small but basic surgical techniques will go a long way in preventing unwanted postoperative events.
[►Fig. 1] and at varying intervals following the CP. Thin skin with lack of subcutaneous support, poor galeal closure, devitalized skin margins due to excessive use of cautery, and tight sutures causing necrosis of the margins are possible causes of incision line breakdown. Repaired lacerations in the middle of the skin flap that was raised during DC lack subcutaneous support, adhere to the "neo dura" and may be devascularized during dissection and elevation of the skin at CP and breakdown later. Most commonly, skin breakdown follows the infection of the operative site.
Di Rienzo et al 6 classified wound complications as being one of three types -dehiscence, ulceration, or necrosis. Dehiscence, the commonest, is the separation of opposing margins along the suture line while ulceration is defined as the loss of substance occurring inside the skin flap distant   from the line of suture and necrosis is a large, discolored area of nonviable skin without exposure of the subjacent bone. 6 These need to be treated promptly as osteomyelitis and spreading infection may ensue. In the absence of infection and if detected, early dehiscence can be managed by debriding the margins until fresh bleeding occurs followed by secondary suturing but in cases who present late there is retraction of the margins and tension free closure is difficult. The conventional notion that an exposed CP must be removed (particularly in cases who present early) needs re-examination given the availability of better antibiotics and improved surgical techniques such as flap coverage. 7 As all our cases presented late, the CP flap was removed and closure with either pulley sutures or rotation flap was done.

Wound Infection
It is the most dreaded complication of CP and ranges from subgaleal pus, intracranial pus below the bone flap (empyema), frank osteomyelitis, or a combination of all of these [►Figs. [2][3][4]. Infections may be classified into early (occurring within 4 weeks of CP) or late (occurring after 4 weeks of CP). 8 Early infections usually present with fever, wound discharge, local swelling, redness and tenderness, and elevated total counts and C reactive protein (CRP) on blood investigations. 8 These may be absent 9 in delayed infections that can even occur several months after the CP. On plain computed tomography (CT) scan imaging, subgaleal pus may be confused with a sterile subgaleal collection but the presence of air must be carefully looked for and if present this hypodensity is often an indicator of infection. 10 Contrast-enhanced CT or magnetic resonance imaging (MRI) scans showing enhancement of the walls of a single or multiseptate collection or restriction on diffusionweighted imaging are confirmatory for the presence of infection. 8 Though it is difficult to identify osteomyelitis unless the bone is grossly eroded because the avascular CP bone does not enhance on contrast we believe the treatment in all cases is re-exploration and removal of the bone flap, thorough debridement and closure to be followed by long-term antibiotics as per culture reports.

Hematoma Below the Replaced Flap
Collection of blood below the CP flap, which is thin and seen in only one to two cuts in a postoperative CT scan is of no clinical consequence. However, on occasion, a large collection may be seen below the replaced bone resulting  in mass effect and midline shift of the underlying brain. 11 Causative factors include bleeding diathesis, improper operative site hemostasis, and a vascular "neo-dura" that is often found in early CPs.
These hematomas are usually extradural while subdural bleed post CP is rare due to the tenuous but well-formed arachnoidal connections traversing the subdural space between the brain and the overlying "neo-dura" that develop following DC essentially obliterating the subdural space.
We have found extradural hematomas to be more frequent in cases where there is an indwelling shunt  [►Fig. 5] or if a lumbar puncture (LP) is done preoperatively to slacken the brain prior to CP as this decreases the natural tamponading effect the latter has on capillary ooze from the dissected neo-dura and also in cases when bone cement used to fashion an artificial bone flap obliterates the temporobasal gap through which any collection can egress to the subgaleal space.
A "wait and watch" policy can be followed if the patient is asymptomatic but significant neurological deficits mandates re-exploration, evacuation of the blood and replacement of the bone flap after drilling a few small holes in it along with drains (in the subgaleal and extradural planes).

Intraparenchymal Hemorrhage
Intraparenchymal hemorrhage after CP can occur due to iatrogenic injury to fragile blood vessels formed following posttraumatic angiogenesis 12 while lifting the skin and galeal flap off the neodura dural cover during exposure or due to screws used to fix the bone [►Fig. 6]. The former etiology is likely to occur more frequently in cases where adequate duraplasty is not done during the initial surgery. 13 Also, negative pressure suction drains might cause traction injury to these vessels.
Hyperperfusion of underlying brain can cause sudden increase in cerebral blood flow once atmospheric pressure is removed following CP and may lead to intraparenchymal bleed particularly in patients with a sunken flap. 14 If the injury is small with no mass effect, midline shift or cisternal effacement on CT scan, conservative treatment may be continued. Surgical evacuation is warranted if the hemorrhage is large and life-threatening and then the bone flap should again not be replaced.

Epidural Fluid Collection/Sub-flap Hygroma
The incidence of epidural fluid collections seen on CT scan below the replaced flap varies from 6.1% to 37.3%. 15 The vast majority are asymptomatic resolving over time. 15,16 They are typically hypodense as opposed to extradural hematomas. Factors such as dural stiffening preventing brain expansion after CP, 15 inflammatory response to artificial bone substitutes, 15 and intraoperative cerebrospinal fluid (CSF) leak have been implicated in its causation. 15,16 When they are large enough to cause mass effect on the brain with fresh deficits [►Fig. 7], treatment options include making a burr hole through the flap to let the fluid out, or craniotomy and evacuation of the collection with placement of subgaleal drain and dural tenting sutures.

Flap Resorption
It is a delayed complication of CP, previously called aseptic necrosis of the bone flap and is of two types 17 -Type 1  where there is thinning of the bone or erosion at the margins of the flap and Type 2 where there is complete lysis of both tables within the flap. The incidence of this complication depends on the length of the follow-up and the attention with which it is sought for and varies from 7.2% to 50%. 17 Multifragmented bone flaps, late CP, larger flaps, younger age of the patient, CP done for trauma, and the presence of a VP shunt have been implicated as predisposing factors for the same. 17,18 Patients present with progressive softening of the operative site and rarely pain and CT scans (with 3D reconstructions) show the extent of resorption [►Fig. 8]. Management options include re-CP with cement or mesh or an expectant "wait and watch" policy in children as recalcification may occur. 19

Flap Mobility
A flap that is not firmly fixed (as with sutures instead of miniplates and screws) may on occasion move with variations in intracranial pressure (occurring with coughing/sneezing) or with posture too. While most patients will have non-serious complaints such as a subjective fullness of the operative site on getting up from sleep which sinks inward somewhat as the day progresses, abnormal mobility of the implanted bone may cause symptoms and called the "Sinking Bone Syndrome." 20 We have documented a case of reversible postural hemiparesis 21 where there was variation in MCA flow with flap movement [►Fig. 9].
Flap mobility can also occur due to incompatible flap size due to its absorption during storage. We have encountered it in cases where we had placed the flap in a subcutaneous abdominal pocket and when the patient underwent a delayed CP [►Fig. 10]. It is probably due to absorption and decalcification of the bone during storage in a metabolically active location. 22

Flap Subsidence
A flap that is inadequately fixed during CP may sink into the brain if LP is done to rule out meningitis [►Fig. 11] or after ventriculoperitoneal shunting. Neurological deterioration may occur due to disturbances in cerebral metabolism (documented using flurodeoxy glucose positron emission tomography studies) due to decreased cerebral blood flow by the pressure of the flap. 21

Extrusion of Implants Used for Fixation
We encountered a previously unreported complication that occurred due to back out of the miniplates and screws used to fix the bone flap during CP with erosion through the skin [►Fig. 12]. Treatment entails removal of the extruded screws

Conclusions
CP is a common but far from uncomplicated surgical procedure. Though we have not analyzed the reason for every complication in each patient, it must be stressed that post-CP complications are myriad and at times may be serious enough to threaten life or warrant resurgery. Attention to small but basic surgical techniques will go a long way in preventing unwanted postoperative events. Fig. 11 Plain skiagrams showing a replaced bifrontal CP flap initially created for hematoma evacuation and clipping of a distal anterior cerebral artery aneurysm at first follow up (A) and immediately following lumbar puncture 6 months later for meningitis (B) following which he became drowsy instantaneously and clinical photograph (C) after lumbar puncture before reinstallation of saline in the thecal sac.